Evidence map›Paper›PMID 25668001›Full record

ReviewNature reviews. Nephrology2015

Sickle cell disease: renal manifestations and mechanisms.

Karl A Nath, Robert P Hebbel

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 6 pooled it
15.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

202 citing papers in PubMed, 6 syntheses or guidelines pooled it, 339 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2023
    Pooled it
  4. Pooled it
  5. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2017
    Pooled it
  6. Pooled it
  7. Trial
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  11. Review
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  16. Observational
  17. Cytochrome bBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Article
  18. Review
  19. Observational
  20. Article

142 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Karl A NathDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, 200 First Street S. W., Rochester, MN 55905, USA.
Robert P HebbelDivision of Haematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, Mayo Mail Code 480, 420 Delaware Street S. E., Minneapolis, MN 55455, USA.
Mayo Clinic · USUniversity of Minnesota · US

Funding

Renal Injury and Adaptation to Heme ProteinsR37DK047060 · NIDDK · MAYO CLINIC ROCHESTER · PI NATH, KARL A. · 2002 to 2011
$3.6M
Mechanism of Dialysis Arteriovenous Fistula DysfunctionR01DK070124 · NIDDK · MAYO CLINIC ROCHESTER · PI NATH, KARL A. · 2005 to 2015
$3.4M
RENAL INJURY AND ADAPTATION TO HEME PROTEINSR01DK047060 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NATH, KARL A. · 1993 to 2018
$2.2M
NIDDK NIH HHS R01 DK047060NIDDK NIH HHS R01 DK070124NIDDK NIH HHS R37 DK047060
6 · The paper itself

Abstract

Sickle cell disease (SCD) substantially alters renal structure and function, and causes various renal syndromes and diseases. Such diverse renal outcomes reflect the uniquely complex vascular pathobiology of SCD and the propensity of red blood cells to sickle in the renal medulla because of its hypoxic, acidotic, and hyperosmolar conditions. Renal complications and involvement in sickle cell nephropathy (SCN) include altered haemodynamics, hypertrophy, assorted glomerulopathies, chronic kidney disease, acute kidney injury, impaired urinary concentrating ability, distal nephron dysfunction, haematuria, and increased risks of urinary tract infections and renal medullary carcinoma. SCN largely reflects an underlying vasculopathy characterized by cortical hyperperfusion, medullary hypoperfusion, and an increased, stress-induced vasoconstrictive response. Renal involvement is usually more severe in homozygous disease (sickle cell anaemia, HbSS) than in compound heterozygous types of SCD (for example HbSC and HbSβ(+)-thalassaemia), and is typically mild, albeit prevalent, in the heterozygous state (sickle cell trait, HbAS). Renal involvement contributes substantially to the diminished life expectancy of patients with SCD, accounting for 16-18% of mortality. As improved clinical care promotes survival into adulthood, SCN imposes a growing burden on both individual health and health system costs. This Review addresses the renal manifestations of SCD and focuses on their underlying mechanisms.

Indexed as

Anemia, Sickle CellDisease ProgressionHumansKidney DiseasesRenal Insufficiency, Chronic

Identifiers

PMID25668001
PMCPMC4701210
OpenAlexW2018424384

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.